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Anti-TSG101 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | Q99816 |
| Host | Rabbit |
| Reactivity | Human, Rat |
| Clonality | Polyclonal |
| Format | Lyophilized |
| Description | Rabbit IgG polyclonal antibody for Tumor susceptibility gene 101 protein(TSG101) detection. Tested with WB in Human;Rat. |
| Reconstitution | Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
| Gene ID | 7251 |
|---|---|
| Other Names | Tumor susceptibility gene 101 protein, ESCRT-I complex subunit TSG101, TSG101 |
| Calculated MW | 43944 MW KDa |
| Application Details | Western blot, 0.1-0.5 µg/ml, Human, Rat |
| Subcellular Localization | Cytoplasm. Membrane; Peripheral membrane protein. Nucleus. Late endosome membrane; Peripheral membrane protein. Mainly cytoplasmic. Membrane-associated when active and soluble when inactive. Depending on the stage of the cell cycle, detected in the nucleus. Colocalized with CEP55 in the midbody during cytokinesis. |
| Tissue Specificity | Heart, brain, placenta, lung, liver, skeletal, kidney and pancreas. |
| Protein Name | Tumor susceptibility gene 101 protein |
| Contents | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3. |
| Immunogen | A synthetic peptide corresponding to a sequence at the C-terminus of human TSG101 (361-390aa KHVRLLSRKQFQLRALMQKARKTAGLSDLY), identical to the related mouse and rat sequences. |
| Purification | Immunogen affinity purified. |
| Cross Reactivity | No cross reactivity with other proteins |
| Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time.Avoid repeated freezing and thawing. |
| Sequence Similarities | Belongs to the ubiquitin-conjugating enzyme family. UEV subfamily. |
| Name | TSG101 |
|---|---|
| Function | Component of the ESCRT-I complex, a regulator of vesicular trafficking process. Binds to ubiquitinated cargo proteins and is required for the sorting of endocytic ubiquitinated cargos into multivesicular bodies (MVBs). Mediates the association between the ESCRT-0 and ESCRT-I complex. Required for completion of cytokinesis; the function requires CEP55. May be involved in cell growth and differentiation. Acts as a negative growth regulator. Involved in the budding of many viruses through an interaction with viral proteins that contain a late-budding motif P-[ST]-A-P. This interaction is essential for viral particle budding of numerous retroviruses. Required for the exosomal release of SDCBP, CD63 and syndecan (PubMed:22660413). It may also play a role in the extracellular release of microvesicles that differ from the exosomes (PubMed:22315426). |
| Cellular Location | Cytoplasm. Early endosome membrane; Peripheral membrane protein; Cytoplasmic side. Late endosome membrane; Peripheral membrane protein. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Midbody, Midbody ring. Nucleus. Note=Mainly cytoplasmic. Membrane- associated when active and soluble when inactive. Nuclear localization is cell cycle-dependent. Interaction with CEP55 is required for localization to the midbody during cytokinesis |
| Tissue Location | Heart, brain, placenta, lung, liver, skeletal, kidney and pancreas |
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Provided below are standard protocols that you may find useful for product applications.
Background
TSG101, known as Tumor susceptibility gene 101, is mapped to 11p15. The protein encoded by this gene belongs to a group of apparently inactive homologs of ubiquitin-conjugating enzymes. The gene product contains a coiled-coil domain that interacts with stathmin, a cytosolic phosphoprotein implicated in tumorigenesis. And the protein may play a role in cell growth and differentiation and act as a negative growth regulator. In vitro steady-state expression of this tumor susceptibility gene appears to be important for maintenance of genomic stability and cell cycle regulation. Mutations and alternative splicing in this gene occur in high frequency in breast cancer and suggest that defects occur during breast cancer tumorigenesis and/or progression.
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